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PSYC 462 > Depression > Flashcards

Depression Flashcards

1
Q

major unipolar depression is one of the most common mood disorders, characterized by ______ mood (absence of happiness), _____, ____ and desperation, loss of ___, _____, _____, appetite, and _____, difficulty in ____ and ____ ____.

A

unhappy, worthlessness, guilt, interest, energy, motivation, pleasure, concentration, restless agitation

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2
Q

depressive episodes that are triggered by external events

A

reactive

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3
Q

when depressive episodes occur without apparent cause

A

endogenous

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4
Q

depression is considered pathological when symptoms are ____ or _____. There is high comorbidity of depression with other medical conditions such as ___ and ____ _____. Symptom clusters vary with individuals and there may be depression ______ associated with distinct causes and pathophysiologies

A

prolonged, disproportionate, anxiety, alcohol dependence, subtypes

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5
Q

Depression increases risk of suicide by ____%

A

7-15

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6
Q

Unipolar depression typically alternates with ____ states, and episodes last up to _____ months. Episodes can recur through life, often increasing in ____ and _____. Sometimes, depressive episodes can end on their own.

A

normal, 6-9, frequency, intensity

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7
Q

______% of the population is affected by depression. ____ are more likely to be diagnosed and incidence often coincides with major ____ changes such as post partum and ____. The incidence of depression has ____ over the last 50 years, and the age of onset has ______. Some types of depression may have a ____ influence, while others less so

A

15-20, women, hormonal, menopause, increased, decreased, genetic

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8
Q

Depression is viewed as a _____ disorder, and is closely related with anxiety. Intense stress and anxiety often ____ depression.

A

stress-linked, precede

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9
Q

Some forms of depression may be linked to alterations in the _______ and higher _____ and ____ levels.

A

HPA-axis, cortisol, CRF

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10
Q

a stress related peptide transmitter in the brain that affects numerous limbic brain regions and stimulates cortisol release

A

CRF

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11
Q

People with ____ ____, which is associated with high levels of glucocorticoids, are more prone to depression

A

cushing’s syndrome

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12
Q

Circulating levels of ____ tend to be higher in depressed subjects vs other disorders and controls.

A

CORT

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13
Q

a synthetic glucocorticoid that can suppress cortisol release in normal people

A

dexamethasone

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14
Q

Dexamethasone can “fool” the HPA axis into believing there are ____ levels of cortisol than normal. Through ____ ____, levels of cortisol drop in healthy control, but not in depressed patients. This is called the _____ _____ ____

A

higher, negative feedback, dexamethasone suppression test

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15
Q

functional imaging studies show increased blood flow / ____ utilization by the ___ and ______. Increased amygdala activity is associated with ____ that may contribute to stress / depressive symptoms. Some aspects of depression may be caused by disrupted regulation of amygdala ___ _____ by the PFC. It may be one mechanism underlying aberrant negative ____ of life events

A

O2, amygdala, vmPFC, anxiety, emotional processing, appraisals

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16
Q

Alterations in brain activity can be normalized with ______ treatment. These regions receive dense _____ and _____ input.

A

antidepressant, noradrenergic, serotonergic

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17
Q

Reduced ____ volumes have also been observed in those with depression

A

hippocampal

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18
Q

model of depression that focuses on the stress-related neuro-endocrine abnormalities of depression

A

glucocorticoid hypothesis

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19
Q

Hypothalamic CRF neurons are regulated by other nuclei: the amygdala ____ it, while the _____ inhibits it. Early life stress can increase CRF expression in the ______, increase amygdala _____ to stress, and decrease ______ ____ in the hippocampus

A

stimulates, hippocampus, hypothalamus, sensitivity, glucocorticoid receptors

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20
Q

Glucocorticoids increase hippocampal ______, and high, _____ levels of intense stress can cause _____ of hippocampal and ____ neurons.

A

excitability, prolonged, atrophy, PFC

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21
Q

impaired hippocampal function leads to the loss of _____ regulation of the HPA axis. It may also contribute to the behavioural syndrome in depression where patients often report being unable to ____ a time when they were happy. Antidepressant drugs reduce ____ levels and reverse loss of hippocampal _______ in animal studies

A

inhibitory, remember, CRF, dendrites

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22
Q

Many animal depression models involve repeated, _____ stressors.

A

uncontrollable

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23
Q

when rodents are exposed to different types of stressors such as cold temperatures, wet bedding, restraint, and sudden loud noise over 1-3 weeks to they cannot habituate to one form of stress

A

chronic mild stress

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24
Q

when an intruder rat or mouse fights a more dominant conspecific - repeated experiences with defeat can induce depression

A

chronic social defeat

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25
Q

when young animals are separated from their mothers for brief periods daily during the first few weeks of life

A

early maternal separation

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26
Q

Forced swim tests in rats or tail-suspension tests in mice model behavioural ______, as ____ is thought to reflect a ____ coping strategy. Acute antidepressant treatment reduces immobility and increases active coping strategies such as ____ and ____ in normal animals

A

despair, immobility, passive, swimming, climbing

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27
Q

typically used with the social defeat model, where rodents avoid conspecifics after repeated defeats

A

social avoidance

28
Q

a behavioural test for depression that models anhedonia - depression reduces preference for sucrose solution vs water; chronic antidepressants can reverse this effect

A

sucrose preference

29
Q

Behavioural tests are routinely used as screens for ____ antidepressants. However, they do not totally translate to ___ observed in human patients. For example, depressed patients still ____ sweet foods if it is presented in front of them, but are less likely to work to obtain them

A

novel, deficits, like

30
Q

Early life stressors can make the HPA axis ______ and increase risk for depression in adult animals. Adults rats subjected to early life trauma showed higher stress-induced ____ and ____ release as adults, and greater ____ behaviours. Antidepressant treatment prevents this increase in adults and _____ the behaviours. When treatment was terminated, all the abnormalities _____

A

over-responsive, CRF, cortisol, depressive-like, prevents, returned

31
Q

in the 1950s-60s, _____ a drug that reduces monoamine levels, was found to induce depression. The first ___ _____ _______, which block metabolism of monoamines and increase brain levels, _____ depression. The first tricyclic antidepressant ______, which blocks monoamine reuptake was also found to be effective. In the 1980s, _____ (SSRI) was found to be effective at treating depression. All of these findings support the ______ hypothesis

A

reserpine, monoamine oxidase inhibitors, alleviate, imipramine, fluoxetine, monoamine

32
Q

the hypothesis that depression is the rsult of abnormal reduction in brain monoamine (mostly 5-HT and NE) levels

A

monoamine hypothesis of depression

33
Q

Some limitations of the monoamine hypothesis are that antidepressants increase monoamine levels ____ yet there is a long lag between the drug treatment and the ____ of symptoms. Thus therapeutic effects may be mediated by longer lasting changes in ___/____ activity and their effects on _____ targets induced by repeated antidepressant treatment (rather than acute increases in NT release). Additionally, not all depressed patients ____ to drugs that increase monoamine levels. antidepressants tend to improve symptoms vs a placebo in more ______ depressed patients, but otherwise there is a large ____ effect. Additionally, depletion of ______ or ____ does not cause a depressive ____ in animal models. These animals instead show some behaviours that may loosely be related to depression such as _____, ______, hypersensitivity to ____ and altered patterns of ____ and ____.

A

quickly, alleviation, NE, 5-HT, postsynaptic, respond, severely, placebo, NE, 5-HT, phenotype, irritability, aggression, pain, feeding sleep

34
Q

another limitation of the monoamine hypothesis is that _____ ______ induces symptoms of depression in unmedicated depressed patients in ____, or healthy subjects with a ____ ___ of depression, but not in healthy subjects without that history. This means merely having low levels of serotonin does not cause depression, except in ____ individuals

A

tryptophan depletion, remission, family history, vulnerable

35
Q

Although the monoamine hypothesis is overly simple, ___ continues to be a focus because of its influence on ____ ____, _____, and response to _____ and _____ events.

A

5-HT, pain sensitivity, emotionality, positive, negative

36
Q

suicide victims and depressed patients show lower _____ _____ and ____ levels taken from post-mortem brains or _____ /______, which is indicative of lower 5-HT activity.

A

5-HT metabolite, precursor, blood, CSF

37
Q

polymorphisms in the _____ gene (short and long) can contribute to depression. The ____ allele is associated with reduced _____ function and ____ levels of 5-HT. These higher levels may reduce firing of 5-HT neurons via _______ inhibition. This may be linked to some forms of depression brought on by ______. Mutant mice _____ for the SERT gene (ie. only having ___ copy of the gene that reduces expression), have lower _____ 5-HT neuron firing rate.

A

SERT, short, transporter, higher, autoreceptor-mediated, stress, heterozygous, 1, raphe

38
Q

_____ depressed individuals show increases in postsynaptic _____ receptors, which may be compensatory to ____ 5-HT activity. Chronic antidepressant treatment ______ the same receptors, in animal and human studies

A

unmedicated, 5-HT2, low, down-regulates

39
Q

In ____ studies, the magnitude of a biological response to 5-HT _____ or ____ is measured. Depressed patients show reduced _____ to 5-HT agonists, and this can be reversed with chronic ______ treatment.

A

challenge, agonist, antagonist, sensitivity, antidepressant

40
Q

acute SSRI treatment increases 5-HT by blocking ____. This in turn, activates ______ _____ to slow cell firing and reduces 5-HT release. Long-term SSRI treatment ______ autoreceptors, so these drugs can increase ______ 5-HT release. For example, ______ _____ autoreceptors become less sensitive to activation following chronic _____ treatment. Repeated SSRI treatment can also increase sensitivity of certain postsynaptic 5-HT receptors in the ____ and _____

A

reuptake, somatodendritic autoreceptors, down-regulates, synaptic, somatodendritic 5-HT1A fluoxetine, PFC, hippocampus

41
Q

NE plays a key role in ____ function, reward ______, _____/_____, and the ____ response. Results of NE _____ and _____ studies of depressed patients show have been inconsistent. One consistent finding is that untreated depressed patients show increased _____ receptors which may attenuate NE release

A

neuroendocrine, mechanisms, attention, arousal, stress, metabolite, receptor, alpha-2

42
Q

Chronic (_____ day) antidepressant treatment in animals downregulates postsynaptic ____ receptors and _____ _______. This lag parallels the onset of the ______ _______. However, this downregulation is not always seen in treated patients

A

7-21, beta, alpha autoreceptors, therapeutic response

43
Q

There are anatomic and functional interactions between NE neurons in the ____ and the 5-HT neurons in the _____, such that drugs that affect one system can affect the other.

A

LC, raphe

44
Q

There is renewed interest in how DA ______ may contribute to depression symptoms, particularly ______ (reduced motivation). _____ ______ ____ are being developed with consideration to not be habit forming like _____

A

dysfunction, anergia, triple-monoamine uptake blockers, cocaine

45
Q

double-blind, placebo controlled trials show that no one drug is more ____ than any other. There is also no way to ____ how a patient will respond to a particular drug. Each patient typically undergoes ____ to find a drug that optimally balances therapeutic vs ____ ___. All drugs require _____ administration and clinical effects depend on _____ changes that takes time to develop

A

effective, predict, trials, side effects, chronic, neural

46
Q

_____/ ____ therapy can be just as effective as antidepressants, although it takes longer, and when used in combination with drugs is even more effective

A

cognitive, behavioural

47
Q

certain drugs, primarily _____, are associated with increased risk of ____ in children and adolescents, but the causal relationship is unclear,

A

SSRIs, suicide

48
Q

first class of drugs used to treat depression; increases the amount of transmitter available for release within hours, but antidepressant effects require weeks of treatment

A

MAO inhibitors

49
Q

examples of MAO inhibitors include _____ (Nardil) _____, (marplan) and _____ (parnate). The use of MAO inhibitors are now limited due to multiple side effects such as _____ disturbances, ___ gain, increase in ____ ___, interaction with other _____ medications, and naturally occurring _____, which can augment NE release and cause dangerous increase in BP. MAO inhibitors also target other _____ ____ that metabolize other drugs

A

phenelzine, isocarboxazid, tranylcypromine, sleep, weight, blood pressure, cold, tyramine, liver enzymes

50
Q

antidepressants that block presynaptic transporters to inhibit reuptake of monoamines, which prolongs the duration of transmitter action at the synapse

A

tricyclic antidepressants

51
Q

Different tricyclic antidepressants have different _____ and ____ reuptake blocking properties. Examples are ____, ____ and _____. Side effects of TCAs include the blocking of ___ receptors, which causes ____ and fatigue, its _____ effects, which causes ___ ___, constipation, urine retention, ____, ____, impaired ____, and ___ ____. Some TCAs also block _____ _____ receptors, and when combined with NE reuptake blocking, may lead to potentially dangerous _____ effects such as ___, ____ and _____. Overdose can cause _____ and ____ depression, _____, convulsions, ____ ___ and coma. TCAs also have a low ____ _____, meaning fatalities occur at approximately ___x the normal therapeutic dose.

A

NE, 5-HT, amitriptyline, desipramine, imipramine, histamine, sedation, anticholinergic, dry mouth, dizziness, confusion, memory, blurred vision, alpha-1 adrenergic, cardiovascular, tachycardia, hypotension, arrhythmia, cardiovascular, respiratory, delirium, cardiac arrest, therapeutic index, 10

52
Q

2nd generation antidepressants that are most commonly prescribed, as the side effect profile is typically better than 1st generation drugs

A

SSRIs

53
Q

The therapeutic effect of SSRIs is mediated by increased activation of some 5-HT receptors. Activation of other receptors can lead to _____, _____ disorders, _____, ____ and ____ dysfunction.

A

anxiety, movement, insomnia, headaches, sexual

54
Q

dangerous effects when SSRIs combined with other 5-HT agonists or drugs that interfere with SSRI metabolism

A

serotonin syndrome

55
Q

serotonin syndrome can lead to ____, ____, _____, ____, fever, ____, diarrhea, increased ___ ____ and ______ ______.

A

agitation, disorientation, ataxia, spasms, shivering, heart rate, blood pressure

56
Q

SSRIs can cause physical ______ and ____ that can last several weeks. This results in ____, ____ vivid ____, increased ____, ____ and _____

A

dependence, withdrawal, fatigue, insomnia, dreams, anxiety, agitation, irritability

57
Q

ketamine is a _____ _____ antagonist. At ______ doses through _____, there is rapid reduction in depressive symptoms for _____% of treatment ______ patients (after psychosis dissipates). Effects last for _____ weeks, and an _____ formula has recently been approved.

A

non-competitive, NMDA, sub-anaesthetic, IV, 7, resistent, 1-3, intra-nasal

58
Q

The mechanism of ketamine appears to be driven by increased ______. It can potentiate ____ receptor function, potentially by increasing ____ and _____ release in the PFC. Administration of ____ ____ ____ prevents the antidepressant response to ketamine in animal models. Ketamine also induces multiple forms of ___ ___ via activation of multiple ___ ___ with effects persisting after acute effects have worn off. Ketamine ____ may also contribute to antidepressant effects

A

excitation, AMPA, glutamate, DA, AMPA receptor antagonists, synaptic plasticity, signalling cascades, metabolites

59
Q

characterized by periods of depression alternating with mania

A

bipolar disorder

60
Q

symptoms of mania include inflated __ _____, reduced need for ____, flight of ____, ______, increased ____ ___ activity, but rarely completed tasks. When mania subsides, difficulties related to behaviour due to mania can trigger bouts of ______.

A

self esteem, sleep, ideas, distractibility, goal directed, depression

61
Q

the cycling ____ of bipolar disorder varies, but rapid cycling consists of ___ or more cycles in one year. Some may cycle several times in one _____. Mania rarely occurs _____.

A

rate, 4, day, alone

62
Q

a milder form of bipolar disorder in which patients cycle between dysthymia (milder depression) and hypomania (increased energy)

A

cyclothymia

63
Q

incidence of mania is considerably ____ than depression. There is a _______% higher prevalence in the U.S. and men and women are affected _____

A

lower, 1-4, equally

64
Q

The neural basis of mania is poorly understood, but may involve pathology of the ____ and ____

A

hippocampus, amygdala

65
Q

the most effective medication for patients with bipolar disorder

A

lithium carbonate

66
Q

lithium carbonate eliminates / reduces ____ episodes without causing depression or producing _____. it has no effect in ____ individuals. It takes ___ weeks for maximal effects to emerge and is particularly effective in reducing ____ in bipolar individuals. Lithium elevates brain _____ _____ levels, and increases _____ ____. At the same time, it reduces ______ activity by enhancing _____ and reducing ____. Lithium likely modifies _____ ___ at points beyond the transmitter receptors (ie. second messenger systems).

A

manic, sedation, healthy, 2-3, suicide, tryptophan 5-HT, 5-HT release, catecholamine, reuptake, release, synaptic transmission

67
Q

the side effects of lithium are generally mild but include increased ___, ____, impaired ___ and ____, fatigue, ____ and ____ gain. Higher levels can be ____ and occur when plasma ____ levels are lower. The ____ ___ is low and thus blood levels of lithium must be ____ regularly.

A

thirst, urination, concentration memory, tremor, weight, toxic, Na+, therapeutic index, monitored

PSYC 462 (16 decks)

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